Bromobenzene toxicity is manifested by both liver and kidney necrosis and also by the covalent binding of radiolabeled bromobenzene to lung tissue. We have shown that a reactive metabolite of bromobenzene, namely the 3,4-oxide generated by hepatocytes, is sufficiently stable to leave cells by trapping it with either externally added protein or with externally added glutathione and glutathionyl transferases. Thus, this intermediate may be responsible for the extrahepatic toxicity observed following bromobenzene administration.